Troubled Sleepers at Risk for Soft Plaque

Action Points

This study found that the frequency of noncalcified/mixed plaques was much higher in patients with obstructive sleep apnea.

Patients also had more severe stenosis and a higher number of involved vessels.

Obstructive sleep apnea has been linked with cardiovascular disease, but it also may be linked with the deadliest type of coronary artery plaque, a small study suggests.

Of patients with obstructive sleep apnea (OSA), 63% had noncalcified or mixed plaques compared with 16% of those without OSA (P<0.0001), according to Sunil Sharma, MD, of East Carolina University in Greenville, N.C., and colleagues.

The unadjusted odds ratio was 9.3 (95% CI 3.0 to 28.4), but even when researchers adjusted for other risk factors, the association of OSA with soft plaque "remained strong" (OR 7.0, 95% CI 1.9 to 26.5, P<0.05), they reported in the study published online in Clinical Cardiology.

"The broad confidence interval was most likely due to small sample size, but we cannot rule out the effect of unobserved confounding factors," researchers noted.

However, Sharma told MedPage Today that the investigators "felt comfortable" with their unique finding regarding more soft plaque in those with OSA because of similar findings linking hard, calcified plaques with OSA.

"We know that hard plaques don't cause acute events. So we wanted to see if those with sleep-disordered breathing had a higher prevalence of soft plaque," Sharma said.

Despite the known connection between sleep apnea and cardiovascular disease, data are limited on whether OSA "causes or accelerates the process of atherosclerosis and plaque formations."

And data are similarly lacking on exactly what type of plaque is most prevalent in those with OSA.

To categorize plaque type, researchers retrospectively reviewed the cardiac CT images of 81 patients who were part of a larger radiology study at the Medical University of South Carolina in Charleston involving emergency room patients with acute chest pain.

All patients had undergone a gold-standard polysomnography test within the prior 3 years of the CT scan, and 51 had OSA.

Baseline characteristics were similar between patients with and without OSA, except in three categories: age (60 versus 54, P=0.05), race (75% white versus 53%, P=0.04), and past smoking (62% versus 39%, P=0.004).

Besides there being an overall strong association of OSA with noncalcified/mixed plaques, the severity of OSA was linearly associated with soft plaques, but the confidence intervals were wide.

Those with an apnea-hypopnea index (AHI) of between 10 and 20 (mild OSA) had an odds ratio of 3.2 (95% CI 0.2 to 43.7) compared with 14.2 (95% CI 1.3 to 158.5) for those with an AHI greater than 20 (moderate to severe OSA). These odds were adjusted for age, sex, race, smoking history, and hypercholesterolemia.

This pattern repeated itself when researchers evaluated patients for multivessel disease and stenosis severity (both P<0.05). Again, however, the confidence intervals were very wide.

Significantly more patients with OSA had multiple coronary artery involvement (85.7% versus 34.5%), which correlated linearly with the severity of apnea (ORs 9.6 for mild OSA and 42.1 for moderate to severe OSA).

Also, more patients with OSA had significantly higher severity of stenosis (22.5% versus 6%), and the severity of artery stenosis correlated with the severity of OSA (7.7% with multivessel disease had mild OSA compared with 24% with severe OSA).

However, the results should be confirmed in larger, randomized studies, he said.

There is speculation that OSA might actually influence the duration of soft plaques, meaning that they stay in a soft stage longer than usual, Sharma said. "But this is mere speculation at this point," he said.

The next steps include determining what impact the higher prevalence of soft plaques has on outcomes and evaluating whether the use of continuous positive airway pressure (CPAP) therapy could make these vulnerable plaques more stable.

There is evidence from carotid ultrasound studies that CPAP therapy is associated with a reduced level of plaque, Sharma said.

Limitations of the current study include its retrospective nature, small number of patients, potential referral bias, and not having data on compliance with CPAP therapy.